Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 18 cases of sarcoidosis, 11 presented with hypercalciuria. Absorptive hypercalciuria was usually involved, but 2 patients had probably a calcium renal leak. Therapy with sodium cellulose phosphate was usually effective in lowering the amount of urine calcium, but thiazides had to be used concomitantly in three cases.
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PMID:Hypercalciuria in sarcoidosis. 61 Jan

In an effort to maintain normal serum calcium levels without inducing hypercalciuria, we treated seven hypoparathyroid patients for up to 25 months with chlorthalidone, a thiazide-like sulfonamide diuretic, plus a salt-restricted diet, without added vitamin D. Mean 24-hour calcium excretion decreased from 179 to 88 mg (P less than 0.001), and mean serum calcium increased from 8.2 to 9.3 mg per deciliter (P less than 0.05). Diuretic therapy or moderate salt restriction alone was not as effective as combined therapy. Beneficial effects were sustained for as long as therapy was maintained. The rise in serum calcium, which involves the filterable and ionized fractions, cannot be due entirely to reduced excretion and may in part be explained by increased intestinal absorption. Oral chlorthalidone plus a low salt diet appears to be an effective alternative to vitamin D in the maintenance therapy of at least some patients with hypoparathyroidism.
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PMID:Treatment of hypoparathyroid patients with chlorthalidone. 62 74

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

The effects of phosphate depletion on magnesium (Mg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell significantly (P < 0.01) from 10.1+/-0.27 (SE) to 5.0+/-0.54 mg/100 ml within 1 day and continued to fall gradually to a level of 1.2+/-0.21 mg/100 ml by the end of the 8th wk. A significant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46+/-2.7 to 126+/-24 mueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300+/-24 mueq/24 h by the 3rd day and remained high ranging between 150-300 mueq/24 h, thereafter. The magnitude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2+/-0.02 to 0.79+/-0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which became evident by the 3rd wk of phosphate depletion. Mg content of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral content because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 mueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or weight of the animals. Our results indicate that phosphate depletion is associated with (a) magnesuria due to a decrease in the net renal tubular reabsorption of Mg with the main source of the urinary losses being bone Mg; (b) hypomagnesemia secondary to the renal leak of Mg; (c) negative Mg balance; and (d) increase in the intestinal fractional absorption of Mg. The latter was not adequate to compensate for the urinary losses of Mg.
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PMID:Effect of phosphate depletion on magnesium homeostasis in rats. 64 Nov 38

A 36-year-old woman suffered from bone pain, muscle weakness, and renal stones after prolonged ingestion of antacids for esophageal reflux. Investigation disclosed hypophosphatemia, hypercalciuria, and osteomalacia by bone biopsy. All symptoms and abnormal laboratory findings reversed with a regimen of oral phosphate supplementation and cessation of antacid intake.
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PMID:Antacid-induced osteomalacia and nephrolithiasis. 64 54

Concentration and excretion in 24-hour urine, as well as serum concentrations of Na, K, Mg, Ca, Cl, P, uric acid and citrate were investigated in 209 calcium oxalate stone patients and 42 stone-free patients. Especially the concentration values of the urine components, except for uric acid and citrate, were found to be significantly lower for calcium oxalate stone patients. 21% of the stone patients showed hypercalciuria; hypercalciuria combined with hyperuricuria was found in only 7.1% of the cases and a solitary hyperuricuria in only 17%. As for kidney cortex, kidney papilla and muscle tissue in 10 calcium oxalate stone patients and 10 stone-free patients, the concentrations of Na, K, Ca, Mg as well as some trace elements were determined quantitatively by means of neutron activation analysis. Statistic analysis yielded a significantly lower sodium content of the kidney cortex within the stone-carrying group. Mean values of the calcium concentration in stone patients were lower for papilla and muscle tissue than in the control group. For magnesium no clear differences were found. The iron content in the papilla and muslce tissue of stone patients was significantly lower.
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PMID:Quantitative element investigations in urine, serum, kidney and muscle tissue of calcium oxalate stone patients. 65 76

A group of 273 children with minor complaints was screened for idiopathic hypercalciuria by measurement of the urine Ca/Cr. Borderline or definitely high levels were noted in 17 of these children, 11 of whom were boys. More intensive metabolic studies were completed on four of these children and on three children who were noted to have symptomatic renal stones associated with idiopathic hypercalciuria. These studies suggest that IH, well recognized in adults, may have its origins in childhood and that appropriate management, if initiated in childhood, may have significant long-term benefits.
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PMID:Idiopathic hypercalciuria in children: prevalence and metabolic characteristics. 66 Mar 55

Polyuria, hyposthenuria, hypomagnesemia, hypercalciuria, advanced nephrocalcinosis, low citrate excretion and low glomerular filtration rates were observed in two female siblings who were followed over 10 years. Acid loading revealed incomplete distal tubular acidosis. Hypomagnesemia was due to renal magnesium wasting. It is suggested that the defect in tubular transport of magnesium is an important factor in the pathogenesis of this syndrome.
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PMID:Renal magnesium wasting, incomplete tubular acidosis, hypercalciuria and nephrocalcinosis in siblings. 66 21

The urinary calcium/creatinine ratio was estimated in two groups of schoolboys--village Arabs and urban Jewish (Ashkenazic) schoolboys, aged 10 to 11 years. Both the mean calcium/creatinine ratio and the frequency of hypercalciuria were higher among the Arab boys, and may be related to the higher incidence of chilidhood urolithiasis in Arab children in Israel.
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PMID:Urinary calcium excretion in schoolboys. Ethnic group differences. 66 19

The prophylaxis of the urinary lithiasis by means of drugs (alkalinisants, Eisemberg's syrup, allopurinol, etc.) obtains a very good result against uric acid and urate stones. The prevention of stones of oxalates, phosphates, carbonates, etc. is possible by trichlormethiazide (if hypercalciuria is present) and especially by a new drug, the Covalitin. Naturally diet and hydrotherapy. Decalogue for the stone's prophylaxis is done.
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PMID:[Prevention of urinary calculi with covalitin and by general measures]. 70 Oct 61


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